Transforming growth factor-beta (TGF-beta) has a dual effect on the proliferation of joint chondrocytes. In medium with a low serum concentration, it inhibits cell growth, while in medium supplemented with 10% fetal calf serum it stimulates cell growth. This stimulation leads to a higher replication rate an a larger number of cells in the G2/M phase of the cell cycle. Since these cells have already replicated their DNA, they can begin mitosis when stimulated by a EGF type factor. This mechanism involves the systems of the TGF-beta receptors which appear to vary with the cell cycle. In addition, a glycane inositophosphate may play a role as a second messenger for TGG-beta in this action. Finally, TGF-beta cannot restore the chondrocyte phenotype in dedifferentiated cells nor limit the dedifferentiation process. It exerts a opposing effect to the deleterious effects of interleukin-1 by inhibiting the expression of the receptors of this cytokine at the level of transcription. These in vitro effects would suggest that TGF-beta plays an important role in the repair potentiality of joint cartilage especially in arthrosis. In vivo studies are however necessary to verify this hypothesis.